Bisht, K and Weigiel, B and Tampe, J and Shing, C and Wagner, KH and Otterbein, L and Bulmer, AC, Biliverdin attenuates LPS-induced pro-inflammatory cytokine expression in whole human blood, Federation of American Societies for Experimental Biology, pp. 649.6. ISSN 0892-6638 (2013) [Conference Edited]
Objective: Inflammation is clearly implicated in the pathogenesis of cardiovascular disease, sepsis and respiratory disorders. The present study aimed to reveal the effect of biliverdin (BV) on the expression of pro/anti-inflammatory cytokines in whole human blood.
Methods: Eight healthy males were recruited and 50 mLs of blood was collected into EDTA vacutainers. Whole blood was supplemented with BV (10 or 50 μM) in the presence or absence of 3 μg/mL lipopolysaccride for 4, 8 and 24 hours. Total RNA was purified at 4 h and plasma was collected at 4, 8 and 24 hours. Gene and protein expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-1Ra and IL-10) were analyzed using qRT-PCR and multiplex Luminex analysis.
Results: Biliverdin inhibited LPS-mediated expression of IL-1 β and IL-1Ra in a dose dependent manner, showing a 50% decrease at 4 h (50 μM, P<0.05). However, BV showed only a slight non-significant decrease (69 %) in IL-6 expression under the same conditions while no significant effect was found for TNF-α and IL-10 expression.
Conclusion: Biliverdin reduces LPS-induced expression of IL-1 β and IL-1Ra in whole human blood. This study is the first translational evidence to support BVís use as anti-inflammatory agent in humans against LPS/sepsis.
|Item Type:||Conference Edited|
|Keywords:||inflammation, cytokine, LPS|
|Research Division:||Medical and Health Sciences|
|Research Group:||Clinical Sciences|
|Research Field:||Clinical Sciences not elsewhere classified|
|Objective Group:||Specific Population Health (excl. Indigenous Health)|
|Objective Field:||Specific Population Health (excl. Indigenous Health) not elsewhere classified|
|Author:||Shing, C (Dr Cecilia Kitic)|
|Deposited By:||Health Sciences A|
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